Abstract
BackgroundHyperandrogenism is the primary manifestation of polycystic ovary syndrome (PCOS), which appears to be caused by excess exposure to androgen. As such, androgenized animal models have been developed and investigated to study the etiology of PCOS. Anti-Mullerian hormone (AMH) is known to be associated with follicle growth, and its levels are two to three times higher in women with PCOS than in those with normal ovaries. We studied how duration of androgen administration affects folliculogenesis and AMH expression.MethodsWe divided 30 immature (3-week-old) Sprague Dawley rats into six groups. Three groups were injected each evening with dehydroepiandrosterone (DHEA) (6 mg/100 g body weight/0.2 ml sesame oil) for 7, 15 or 30 days, respectively. The three control groups were injected with 0.2 ml of sesame oil for the corresponding lengths of time. Resected ovaries were sectioned and examined to determine follicle numbers at each developmental stage, and immunostained to assess AMH expression.ResultsOn day 7, follicle numbers and AMH expression levels at each developmental stage of follicle growth were similar in the respective control and DHEA groups. On day 15, the total follicle number (P = 0.041), the percentage of primordial follicles (P = 0.039) and AMH expression were significantly greater in the DHEA than the control group. On day 30, the percentages of primordial (P = 0.005), primary (P = 0.0002) and atretic (P = 0.03) follicles were significantly greater in the DHEA group, whereas the percentage of intermediary follicles (early pre-antral, late preantral, and early antral follicles) was significantly lower in the DHEA group (P = <0.0001). AMH expression in DHEA-treated rats on day 30 was seen exclusively in the primordial (P = 0.0413) and late antral follicles (p = 0.028).ConclusionsAndrogen administration increases AMH production in a process that regulates the growth of primordial follicles. That is, androgen-induced AMH expression provides local negative feedback to folliculogenesis augmented by androgen.
Highlights
Hyperandrogenism is the primary manifestation of polycystic ovary syndrome (PCOS), which appears to be caused by excess exposure to androgen
Examination of the histology of ovaries in androgen-administered female-to-male transsexual (FTM) patients revealed increased follicular atresia, though the morphogenesis of polycystic ovaries is controversial [3,8,9]. Judging from these findings, it appears that androgen administration may impact folliculogenesis and subsequent ovarian morphology, leading to the development of the PCO morphology, but the effects of exogenous androgens on ovarian morphology may vary depending on the period and duration of the androgen administration and the amount of hormone administered
The increased Anti-Mullerian hormone (AMH) production is observed in PCOS [19], which supports the premise that the elevated AMH in PCOS is caused by hyperandrogenemia
Summary
Hyperandrogenism is the primary manifestation of polycystic ovary syndrome (PCOS), which appears to be caused by excess exposure to androgen. The polycystic ovary (PCO) morphology in PCOS is characterized by an excessive number of growing follicles, suggesting folliculogenesis is Several androgenized animal models have been developed and investigated to determine the etiology of PCOS. Examination of the histology of ovaries in androgen-administered FTM patients revealed increased follicular atresia, though the morphogenesis of polycystic ovaries is controversial [3,8,9] Judging from these findings, it appears that androgen administration may impact folliculogenesis and subsequent ovarian morphology, leading to the development of the PCO morphology, but the effects of exogenous androgens on ovarian morphology may vary depending on the period and duration of the androgen administration and the amount of hormone administered. Androgen-induced PCO morphology may be a timelapse snapshot of metamorphosis
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